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aPATH P COPY (SC) > Cell injury > Flashcards

Cell injury Flashcards

1
Q

Severe changes in the environment lead to

A

cell adaptation, injury or cell death.

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2
Q

Degree of injury depends on:

A

Type of injury

Severity of injury

Duration of injury

Type of tissue

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3
Q

What can causes injury to a cell?

A
  • Hypoxia
  • Toxins
  • Physical agents
    • Direct trauma
    • Extreme temp
    • Changes in pressure
    • Electric currents
    • Radiation
    • Microorganisms
    • Immune mechanism
    • Dietary insufficiency and deficiency’s, dietary excess
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4
Q

Cell components most susceptible to injury

A

1. Cell membranes

  • Plasma membrane
  • Organelle membrane

2. Nucleus

  • DNA

3. Proteins

  • Structural (enzymes)

5. Mitochondria (oxidative phosphorylation)

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5
Q

How does the immune system damage the body’s cells?

A

Hypersensivity reactions

Autoimmune reactions

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6
Q

Hypersensivity reactions

A

host tissue is injured secondary to an overly vigorous immune reaction e.g. urticaria (hives)

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7
Q

Autoimmune reactions

A

immune system fails to distinguish self from non-self e.g. Graves disease of thyroid

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8
Q

hypoxia is due to

A

ischaemia

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9
Q

ischaemia

A

is insufficient blood flow to provide adequate oxygenation.

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10
Q

causes of hypoxia

A

hypoxaemic hypoxia

anaemic hypoxia

ischaemic hypoxia

histotoxic hypoxia

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11
Q

Hypoxaemic hypoxia

A

-arterial content of oxygen is low

  • Reduced inspired pO2 at altitude
  • Reduced absorption secondary to lung disease
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12
Q

Anaemic hypoxia

A

decreased ability of haemoglobin to carry oxygen

  1. Anaemia
  2. CO poisoning
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13
Q

Ischaemic hypoxia

A

interruption to blood supply

  1. Blockage of a vessel
  2. Heart failure
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14
Q

Histotoxic hypoxia

A

inability to utilise oxygen in cells due to disabled oxidative phosphorylation enzymes

  1. Cyanide poisoning
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15
Q

hypoxia can be

A

reversible or irreversible (if prolonged)

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16
Q
A
  1. Ischaemia causes a reduction in oxidative phos in the mitochondria
  2. Less ATP produced
  3. Reduced Na pump = influx of calcium, H2O and Na+, effluent of K+
    1. cellular swelling
    2. Loss of microvilli
    3. Bless
    4. ER swelling
    5. Myelin figures
  4. Increased glycolysis
    1. decreased pH (cli]umping of nuclear chromatin)
    2. Decreased glycogen 5) other affects
    3. detachment of ribosomes
    4. Decreased protein synthesis
    5. Lipid depositor
  5. Decreased protein synthesis
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17
Q

prolonged hypoxia is

A

irreversible

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18
Q

characteristics of injured/dying cell

A
  • cytoplasmic changes
  • nuclear changes
  • abnormal cellular accumulations
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19
Q

blebs

generalised swelling

A
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20
Q

nuclear changes

A
  • abnormal clumping of nuclear chromatin
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21
Q

Abnormal cellular accumulations

A
  • dispersion of ribosomes, swelling of mitochondria and ER
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22
Q

alive vs injured vs dead cells

A
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23
Q

Pyknosis

A

is the irreversible condensation of chromatin in the nucleus of a cell undergoing necrosis or apoptosis. It is followed by karyorrhexis, or fragmentation of the nucleus.

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24
Q

Karyorrhexis

A

is the destructive fragmentation of the nucleus of a dying cell whereby its chromatin is distributed irregularly throughout the cytoplasm.

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25
Q

karyolysis

A

dissolution of a cell nucleus, especially during mitosis.

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26
Q

other causes of cell injury

A

extreme cold and free radicals

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27
Q

definition of a free radicale

A

Single unpaired electron in an outer orbit- unstable configuration hence reacts with other molecules–>producing further free radicals

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28
Q

examples of reactive oxyen species

A

• OH• (hydroxyl) - the most dangerous

  • O2- (superoxide)
  • H2O2 (hydrogen peroxide)
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29
Q
A
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30
Q

Exogenous factors which increase formation of free radicals

A
  • Smoking
  • Ionising radiation
  • Air pollution
  • UV light
  • Inflammation
  • Metabolism
31
Q

formation of free radical

A
  • Normal metabolic reactions e.g. oxidative phosphorylation
  • Inflammation- oxidative burst of neutrophils
  • Radiation
  • Contact with unbound metals within the body: iron (by Fenton reaction) and copper
    • Free radical damage occurs in hemochromatosis and Wilsons disease
  • Drugs and chemicals e.g. the liver during metabolism of paracetamol or carbon tetrachloride by P450 system
32
Q

how do free radicals injure cells?

A

Most important targets are lipids in cell membranes

Also oxidise proteins, carbohydrates and DNA

33
Q

how do free radicals damage lipids in the cell membrane

A
  • Cause lipid peroxidation
  • This leads to generation of further free radicals –> autocatalytic chain reaction
34
Q

ROS oxidise proteins, carbohydrates and DNA

A

These molecules become bent out of shape, broken or cross-linked

Mutagenic and therefore carcinogenic

35
Q

how does the body control free radicals?

A

1. Anti-oxidant scavengers

  • Donate electrons to the free radical
  • e.g. Vitamin A, C and E

2. Metal carrier and storage proteins

  • transferrin, ceruloplasmin –> sequester ion and copper

3. Enzymes that neutralise free radicals

  • superoxide dismutase
  • catalase

- glutathione peroxidase (GSH)

36
Q

abnormal cellular accumulations

A

When metabolic processes become deranged:

  • Sublethal or chronic injury
  • Can be reversible
  • Can be harmless or toxic
  • Derived from:
  • Cells own metabolism
  • Extracellular space e.g. spilled blood
  • Outer environment e.g. dust
37
Q

Mechanisms of intracellular accumulations

A
  • Abnormal metabolism
  • Alterations in protein folding and transport
  • Deficiency of critical enzymes
  • Inability to degrade phagocytosed particles
38
Q

What can accumulate?

A
  • Fluid
  • Lipids
  • CHO
  • Proteins
  • Pigment
39
Q

(1) Fluid accumulation in cells

A
  • Hydropic swelling
  • Occurs when energy supplies are cut off e.g. hypoxia
  • Indicates severe cellular distress
  • Na+ and water flood into cell
40
Q

where is fluid accumulation in cells particularly dangerous

A

Particular problem in the brain

41
Q

(2) Lipid accumulation in cells

A

Steatosis (accumulation of triglycerides)

42
Q

where is lipid accumulation in cells often seen

A

in the liver (major organ of fat metabolism)

  • if mild asymptomatic
43
Q

causes of lipid accumulation

A
  • Alcohol
  • Diabetes mellitus
  • Obesity
  • Toxins (carbon tetrachloride
44
Q

what does steatosis look like?

A
45
Q

(3) Protein accumulation in cells is seen as

A

eosinophilic droplets or aggregations in the cytoplasm

46
Q

examples of when protein accumulates in cells

A

alcohol liver disease

alpha-1-antitrypsin deficiency

47
Q

alcohol liver disease

A

Mallorys hyaline (damaged keratin filaments)

48
Q

α1-antitrypsin deficiency

A
  • Liver produces incorrectly folded α1-antitrypsin protein (a protease inhibitor)
  • Cannot be packaged by ER, accumulates within ER and is not secreted
  • Systemic deficiency – proteases in lung act unchecked resulting in emphysema
49
Q

(4) Exogenous and endogenous pigment accumulation in cells

A
  • Carbon/coal dust/ soot- urban air pollutant
  • Inhaled and phagocytosed. By alveolar macrophages
  • Anthracosis and blackened peribronchial lymph nodes
  • Usually harmless, unless in large amounts
    • Fibrosis
    • And emphysema (coal workers pneumoconiosis)
50
Q

Other examples of exogenous

A
  • Tattooing- pigments pricked into skin
  • Phagocytosed by macrophages in dermis and remains there
  • Some pigment will reach draining lymph nodes
51
Q
A
52
Q

endogenous pigment accumulation in cells

A

hemosiderin

53
Q

hemosiderin

A
  • Iron storage molecule
  • Derived from Hb- yellow/ brown
  • Forms when there is systemic or local excess of iron e.g. bruise
  • With systemic overload of iron, hemosiderin is deposited in many organs = hemosiderosis
  • Seen in haemolytic anaemias, blood transfusions and hereditary hemochromatosis
54
Q

Hereditary haemochromatosis

A
  • Genetically inherited disorder - results in increased intestinal absorption of dietary iron
  • Iron is deposited in skin, liver, pancreas, heart and endocrine organs - often associated with scarring in liver (cirrhosis) and pancreas.
55
Q

symptoms of Hereditary haemochromatosis

A
  • liver damage
  • heart dysfunction
  • multiple endocrine failures- especially of the pancreas.
    • was called ‘bronze diabetes’
56
Q

Treatment of Hereditary haemochromatosis

A

is repeated bleeding

57
Q

jaundice

A

Accumulation of bilirubin – bright yellow

Breakdown product of heme, stacks of broken porphyrin rings

Formed in all cells of body (cytochromes contain heme) but must be eliminated in bile

58
Q

jaundice is the

A

accumulation of bilirubin- bright yellow

59
Q

bilirubin is the

A

product of heme- stacks of broken prophyrin rings

60
Q

haem is taken from tissues by

A

albumin to the liver- iron is recycled and haem becomes bilirubin.

bilirubin becomes conjugated with glucoronic acid to become bile

61
Q
A
62
Q

unconjugated bilirubin transported in the blood bound

A

to albumin

  • when in excess can cause jaundice
63
Q

When membranes are leaky can molecules leak out as well??

A

Yes- can have both local and systemic effects

  • local inflammation
  • may have general toxic effects on body
  • May appear in high conc in blood and can aid in diagnosis
64
Q

examples of molecules which can leak out of the cell if damaaged

A
  • Enzymes
    • CK
    • AST
    • Troponin
  • Myoglobin
    • Rhabdomyolysis
  • Potassium
65
Q

pathological calcification

A
  • Abnormal deposition of calcium salts within tissues
  • Can be localised (dystrophic) or generalised (metastic)
66
Q

dystrophic calcification is much more

A

common than metastatic

67
Q

where does dystrophic calcification occur?

A
  • in area of dying tissue
  • atherosclerotic plaques
  • ageing of heart valves
  • in tuberculus lymph nodes
  • some malignancies
68
Q

causes of dystrophic calcification

A
  • No abnormality in calcium metabolism- or serum calcium or phosphate conc
  • Local change/disturbance
  • Favours nucleation of hydroxyapatite crystals
69
Q

dystrophic calcification can cause

A

organ dysfunction e.g. atherosclerosis or calcified heart valve

70
Q

Causes of metastatic calcification

A
  • Due to hypercalcaemia secondary to disturbances in calcium metabolism
  • Hydroxyapatite crystals are deposited in normal tissues throughout the body
  • Usually asymptomatic but it can be lethal
  • Can regress if the cause of hypercalcaemia is corrected
71
Q

causes of hypercalcaemia

A
  • Increased secretion of parathyroid hormone (PTH) resulting.
  • Destruction of bone tissue
72
Q

Increased secretion of parathyroid hormone (PTH) resulting. In bone resorption:

A
  • Primary- due to parathyroid hyperplasia or tumour
  • Secondary- due to renal failure and retention of phosphate
  • Ectopic- secretion of PTH related protein by malignant tumours (carcinoma in lungs)
73
Q

destruction of the bones

A
  • Primary tumours of bone marrow, e.g., leukaemia, multiple myeloma
  • Diffuse skeletal metastases
  • Paget’s disease of bone – when accelerated bone turnover occurs
  • Immobilisation

aPATH P COPY (SC) (19 decks)

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